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Na~+-K~+-ATP酶抑制与心肌缺血后再灌注性损伤

Na~+-K~+-ATPase INHIBITION AND POST-ISCHEMIC REPERFUSION INJURY

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【作者】 赵廷存徐海时安云

【Author】 Zhao Tingcun, Xu Hai, Shi Anyun (Department of Pathophysiololgy, Beijing Medical University, Beijing 100083)

【机构】 北京医科大学病理生理学教研室北京医科大学病理生理学教研室 北京 100083北京 100083北京 100083

【摘要】 在离体大鼠心脏灌流模型上,观察细胞内高钠对心肌缺血后再灌注性损伤的影响。在低灌流过程中,给予Na+-K+-ATP酶抑制剂哇巴因造成细胞内高Na+,可加重缺血后再灌注心脏的血液动力学障碍;增加心肌组织丙二醛含量及冠脉流出液中乳酸脱氢酶的活性;降低线粒体及胞浆液中谷胱甘肽过氧化物酶活力;并使心肌组织中Ca2+超负荷及K+丢失严重。因此,细胞内高Na+可能是心肌缺血后再灌注损伤的基础。

【Abstract】 The detrimental effects of ouabain on post-ischemic myocardium were observed in the model of ischemic-reperfusion injury in isolated rat hearts. Ouabain was added to anoxic Krebs-Henseleit solution during low flow perfusion. As compared with the control group, ouabain caused additional increase in Na+ after reperfusion, associated with depression of ventricular function, Ca2+ overload, loss of K+, increase in MDA contenty and LDH activity and decrease in GSH-Px activity. These results suggest that Na+ overload induced by ouabain may play a certain role in the mechanism of ischemic reperfusion injury.

  • 【文献出处】 中国应用生理学杂志 ,Chinese Journal of Applied Physiology , 编辑部邮箱 ,1993年01期
  • 【被引频次】2
  • 【下载频次】41
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